BMB 6 Flashcards

1
Q

What two processes in the brain maintain adequate bloodflow?

A

1) autoregulation

2) local metabolites like co2

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2
Q

urgent vs emergency HTN? in terms of sx and tx?

A

both are 180/120 mm hg, diff is that emergent has acute end organ damage such as brain swelling/bleeding and fluid in lungs or aortic dissection/MI
-tx: for urgent, immediate with oral meds, usu no hospitalization, but emergent has hospitalization in ICU and IV meds

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3
Q

What is the critical range of blood pressure in which autoregulatory (vasculature maintanence of constant blood flow) mechanisms work?

A

50-150mm hg, plateau on graph of CBF
If bp too high, arterioles vasconstrict to reduce blood flow, but if hypotnesive, then dilate (but in extreme HTN, presssure is higher than autoreg range so arterioles end up vasodilating and “breaking through” plateau)

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4
Q

How does an increase vs decrease on CO2 modify autoregulation?

A

INcrease in CO2 (hypercapnia) shifts curve up and left to get rid of CO2 (so CBF increases, vasodilation) to get rid of co2. Reduced autoregulatory range, breakthrough point occurs sooner/at lower pressures

-decrease in CO2 means curve goes down and right with incr autoreg range, produces vasocon to hold onto co2

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5
Q

How does mean arterial BP affect autoreg?

A

in HTN (incr in MAP), CBF is generally decreased because the lumen diameter is decr

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6
Q

What happens to autoreg mechs after stroke?

A

Impaired!, blood flow pressure passive, myogenic sys dmged, METABOLISM DRIVES CBF
-focal metabolic coupling: all major metabolites are vasodilators, blood flow will oversupply these and o2 after stroke then release will go back to normal

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7
Q

How do glial cells affect local brain blood flow?

A
  • glial cells are around vessels/capillaries, regulate EC K+ (by taking it up and resdistributing it to other areas) thus protect cell from depol so prevent it from being hyper excitable aka causing seizures (also take up glutamate and convert it)
  • they can also swell by taking up excess fluid via aquaporins to protect neurons from swelling
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8
Q

What is and isnt the major regulatory molecule to regulate CBF?

A

CO2 is, O2 is not unless in severe hypoxia (diff from periph circ/chemorec that do respond to O2)

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9
Q

In which pop is decr in cerebral met and decr in blood flow most likely to occur?

A

loss of neurons in elderly w atherosclerosis, >25

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10
Q

What 2 features of EEG are we most interested in?

A

amp and freq

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11
Q

What does amp in eeg depend on (2 factors

A

number of active elements (action/syn potls) and synchrony (incr amp)

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12
Q

Why are synaptic potentials more impt than ap (and greater contributor to EEG spikes and waves?)

A

glial cells, slower and better picked up by EEG

EEG has small amp with greater distance traveled

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13
Q

which bands of waves are teh slowest? which are seen in the HC? whcih are made with eyes closed and slow? which rep awake activity

A

delta- slowest, deep sleep, lowest freq
theta-seen in HC
alpha- eyes closed/drowsy, more regular
beta- mixed is awake, high freq

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14
Q

Evoked potential–what is the purpose of it/what does it test

A

reflect stimulation and tests sensory pathway in patient eg who is comatose, used often in the SC bc more sensitive than MRI, also assess vis/aud pathways in kids

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15
Q

Epilepsy def

A

seizures that occur more than once and other causes can be ruled out (paroxysmal) (ictal means seizure), circuitry/synaptically driven event ((propensity to seize unprovoked)

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16
Q

What is the general progression graph of a seizure

A

PDS (paroxysmal depol shift) wave, with ap’s, then prolonged hyperpol (silent period), tonic then clonic phase, the post ictal depr (may have muscle weakness that mimics stroke)

17
Q

What does tonic clonic seizure involve

A

tonic- continual muscle quivering, clonic- periodic jerking (clonus=spasm)

18
Q

What is a grand mal seizure

A

involves both hemis thus loss of consciousness, generalized seizure example with motor manifestations

19
Q

Causes of seizures w homeostatic disruption

A

trauma, can take long time to appear, drug tox/withdrawals, if no prior history of trauma in adult, could be tumor/stroke
-channelopathies with alterations in v gated channels which can cause hyperexcitability etc
usu idiopathic
infection in infant etc etc

20
Q

how do you dx seizure

A

must be eeg and video recording

21
Q

do all seizures have motor component?

A

no!

22
Q

What are the two categories of seizures, and the two subcategories of each?

A

1) Generalized and 2) partial
2 types of generalized are CONVULSIVE and NON-convulsive
partial seizures can be simple and complex (focal area of brain)

23
Q

What do the types of generalized seizures involve?

A

inv entire brain
conv- have motor components, bc when stim fires easily (motor cortex sus to seizures), and non-conv- show alterations in consciousness/beh

24
Q

Ways to trigger seizures to get recording on EEG

A

hyperventilation-blow of Co2 to cause cortical hyperexcitability
photic stim- flashes of light
methohexita- short acting barb to enhance brain excit
sleep- prone to seizures in transitions between sleep and wake

25
Q

Tonic vs clonic seizure graph and sx

most common

A

tonic- lots of little quivering in graph, very dense, person is in kinda fixed position and stretched out, whereas clonic involves more alternations between quiet parts and peaks in graph, person is scrunched and jerking

26
Q
status epilepticus
def
what to do
complications
what's happening w neurons
A
  • repetitive seizures w/o complete recovery in between, or seizure lasting longer than 5 min -high mort, MEDICAL EMERGENCY, can cause pulm and CV issues and DIC etc etc
  • Stop seizure with anticonvulsant or anesthesia
  • Both autonomic divisions activated, brains req for blood and O2 greatly increase during seizure where anoxemia is produced, need to meet demands)
27
Q

Petit mal seizures, sx etc

A

no prodromal warning, sudden onset, then go back to normal (generalized seizure), usu arise in kids at first, can be lots per day but lasting a few sec, lose consciousness during

28
Q

focal seizures sx and graph

A

activity spreads from one area to another, jacksonian progression of sx, usu start with aura, graph has FOCAL SPIKES/ SHARP WAVES and progression of sx

29
Q

What is the most common type of focal seizure?

A

Psychomotor/temporal lobe seizure:
progression of sx inv HC (susceptible region), inv alteration of csonciousness but may have normal ish behaviors that are out of context (picking at clothing, staring, complex emotional feelings), spread to other area

30
Q

Most common place for seizure to arise?

A

temporal lobe! such as HC

dont occur in cerebellum

31
Q

What is spreading depression?

A

proound depol where memb gets leaky to all ions and pumps cant keep up so ions run downhill (can recover with lots of met energy, or else irrev), nernst potls approach 0

32
Q

Migraine sx

A

start with aura but diff seizure, occip cortex aura causing vis disturbances (in seizure is usu smell), depr of EEG activity spreads (SD) from depol, vascular changes which contr to headache (lots of met energy, dilation/constr of vessels)
seq: hypoperf, aura, headache, hyperperf

33
Q

migraine stages

A

prodrome- can last hours to days, difficult conc, yawning or fatigue, light/noise sens
aura- vis illusions of lights and sparks etc, followed by blind spots, lasts up to an hr
headache- pain and light/sound sens, N/V, hours to days
postdrome- still sens, fatigue, zombie phase, hours to days